Download Treatment of peptic ulcer disease

Gastrointestinal disorders
Prepared by:
Dr. Nehad Jaser
Introduction
 The gastrointestinal (G.I.) tract comprises the oral cavity,
esophagus, stomach, small intestine (duodenum,
jejunum, ileum) and large intestine (colon and rectum).
 Accessory organs such as the pancreas, liver and
gallbladder play an important role in the digestive
process.
 The process of digestion begins in the mouth with the
mechanical grinding of food by the teeth.
 Saliva produced by the salivary glands lubricates the
food and contains amylase enzymes that begin the
digestion of starches.
 The chewed food or chyme now passes down the
esophagus and enters the stomach. In the stomach, the
chyme is further broken down by highly acidic gastric
juice produced by the stomach lining.
 The enzyme pepsin is released by cells in the stomach
lining to begin digestion of proteins.
 Muscular contractions of the stomach wall also serve to
further grind the chyme into a smooth liquid. The chyme
is now driven into the small intestine by contraction of
the stomach.
 In the small intestine, further digestion of proteins,
sugars will occur via intestinal and pancreatic enzymes.
 The small intestine is also where the majority of nutrient
absorption occurs.
 By the time the remaining chyme has reached the large
intestine, most of the available nutrients have been
absorbed from it.
 The large intestine functions mainly in the absorption of
water as well as the synthesis of vitamin K and certain B
vitamins.
General Symptoms of G.I. Disease





Anorexia — loss of appetite
Nausea
Vomiting
Diarrhea, constipation
Bleeding
Abnormalities of the esophagus
Dysphagia
 Difficulty swallowing that may be caused by obstruction
of the esophagus or impaired motility of the esophageal
walls.
 Obstruction may be caused by tumors, congenital
narrowing .....etc
 Neurologic disorders such as brain injury, stroke may
affect voluntary swallowing or peristalsis of the
esophagus.
Gastroesophageal reflux disease
 Gastroesophageal reflux is a condition caused by
the backflow of stomach contents into the
esophagus.
 It results from weakness or incompetence of the
lower esophageal sphincter that normally blocks
reflux of stomach contents into the esophagus.
 Because of their high acid content (low pH), reflux of
stomach contents will cause irritation and
inflammation of the esophagus (esophagitis) that
can lead to ulceration of the esophagus.
 A hiatal hernia may also cause gastroesophageal
reflux. A hiatal hernia is a protrusion of the top of the
stomach through the opening of the diaphragm.
Manifestations
 Burning pain in the epigastric region (“heartburn”) that
may be worsened by alcohol consumption, caffeine,
smoking, exercise and obesity.
 Reflux may also be worsened by lying down.
 Esophagitis, possible ulceration of esophagus.
 Dysphagia, poor nutrition.
 Possible increased risk of esophageal cancer with
chronic esophagitis.
Treatment
 Consumption of frequent small meals rather than large
ones.
 Sleeping with head elevated.
 Consumption of fluids with meals to wash food out of the
esophagus.
 Use of antacids or proton pump inhibitors to reduce pH
of stomach contents.
 Surgery if a hiatal hernia is present.
Disorders of the stomach
Gastritis
 Gastritis refers to inflammation of the gastric mucosa
(stomach lining).
 It may present as an acute or chronic disorder.
Acute gastritis
 Transient irritation and inflammation of the stomach
lining.
 May be caused by factors such as alcohol consumption,
aspirin use and stress.
 The inflammation associated with acute gastritis is a selflimiting process that does not usually result in long-term
injury to the gastric mucosa.
Chronic gastritis
 Chronic irritation and inflammation of the stomach lining.
 May be caused by bacterial infection, alcohol abuse or
long-term aspirin and nonsteroidal anti-inflammatory
drug (NSAID) use.
 Can lead to atrophy and ulceration of the gastric
mucosa.
Peptic ulcers
 Peptic ulcer disease is a general term for ulcers that
occur in the stomach or duodenum (upper part of the
small intestine).
 If the ulcer occurs in the stomach lining, it is specifically
referred to as a gastric ulcer.
 In the United States most ulcers occur in the duodenum
and in elderly patients.
 Peptic ulcers that occur on the inside of the stomach are
called gastric ulcers.
 Peptic ulcers that occur inside the hollow tube
(esophagus) are called esophageal ulcers.
 Peptic ulcers that affect the inside of the upper portion of
your small intestine (duodenum) are called duodenal
ulcers.
Pathogenesis of peptic ulcer

 Peptic ulcers are produced by an imbalance between the
Protective Factors and Hostile Factors
The causes of peptic ulcer disease include the following:
 Infection with the bacteria Helicobacter pylori occurs in 80 to 95% of
patients with peptic ulcer disease.
 Excess acid production from gastrinomas, tumors of the acid
producing cells of the stomach that increases acid output .
 Chronic use of aspirins and NSAIDs.
Manifestations of peptic ulcer disease
 Episodes of remission and exacerbation
 Pain
 G.I. bleeding and possible hemorrhage (20 to 25% of
patients)
 Perforation of ulcers with significant mortality
 Obstruction of G.I. tract
Treatment of peptic ulcer disease
 Avoidance of alcohol, smoking and NSAIDs
 Antibiotics for eradication of H. pylori if present
 Antacids (Examples: magnesium hydroxide , aluminum
hydroxide )
 H 2 receptor antagonists (examples: Ranitidine ,Cimetidine )
 Proton-pump inhibitors (example: Omeprazole)
 Mucosal protective agents (examples: bismuth , sucralfate )
Disorders of the intestines
Disorders of the intestines
Irritable bowel syndrome
 May be one of the most common G.I. disorders.
 Patients present with symptoms of G.I. pain, gas,
bloating and altered bowel function (diarrhea or
constipation). Most symptoms are localized to the lower
intestine and colon.
 No underlying pathophysiologic processes have yet to
be identified in these patients. “Hyperreactivity” and
excessive motility of the bowels may be contributing
factors.
 Emotional factors and diet may exacerbate the
symptoms.
 Treatment may include psychological counseling, dietary
changes such as increased fiber consumption.
Antidiarrhea, anticholinergic and antispasmodic agents
might also be of value.
Inflammatory bowel disease
 The term inflammatory bowel disease includes the
conditions Crohn’s disease and ulcerative colitis . Both of
these diseases are characterized by chronic
inflammation of various regions of the G.I. tract
Crohn’s disease
 Although the exact etiology of Crohn’s disease in
unknown, there appears to be a significant autoimmune
component. Much recent interest has focused on the
possible role of pro-inflammatory cytokines in the
pathogenesis of this disorder.
 The disease may affect any region of the G.I. tract but is
most commonly seen in the distal ileum and colon.
 Distribution of Crohn’s disease shows a distinct
predisposition to certain populations including Jews and
individuals from the United States, Western Europe and
Scandinavia.
 The disease often presents in the late teens to early 20s
and is present for the life of the patient with intermittent
periods of remission and exacerbation.
 The inflammation of Crohn’s disease is particularly
evident in the submucosal layer of the intestine.
 The inflammatory lesions are not constant along the
length of the intestine but rather present with a “skip”
pattern that disperses areas of inflammation with normal
looking, non-inflamed tissue.
Manifestations of Crohn’s disease
 Diarrhea (blood is usually not evident in the stool but may be occult,
i.e., detected by clinical assay)
 Intestinal pain similar to indigestion
 Fever
 Weight loss from intestinal malabsorption
 Nausea, anorexia, vomiting
 Complications: intestinal obstruction, formation of fistulas (abnormal
connections between the colon and other abdominal organs)
 Toxic megacolon
Toxic megacolon
 Life-threatening distention of the colon.
 May lead to perforation of the colon, septicemia and
peritonitis.
 Mortality associated with a perforated colon is on the
order of 40% or more.
Treatment of Crohn’s disease
 Nutritional supplementation to offset the poor nutrition
that can result from anorexia and intestinal
malabsorption. Total parenteral nutrition may be
indicated in severe cases.
 Anti-inflammatory drugs.
 Recently, considerable research has focused on the role
of pro-inflammatory cytokines in Crohn’s disease and the
possibility that drugs or antibodies that block cytokine
action might be of benefit in treating the disease.
Ulcerative colitis
 Inflammatory disease of the rectum and colon.
 The disease primarily affects the submucosa layer of the
intestines.
 Unlike Crohn’s disease the pattern of inflammation is
continuous throughout the affected area.
 Like Crohn’s disease, ulcerative colitis also presents with
periods of remission and exacerbation.
 Although the exact etiology of ulcerative colitis is
unknown, genetic and immunological factors are likely
contributors to the disease.
 Individuals between the ages of 20 and 40 are most
susceptible, particularly those with a family history of the
disorder or who are of Jewish descent.
Manifestations of ulcerative colitis





Chronic, bloody diarrhea
Fever, pain
Weight loss
Possible anemia from blood loss
Possible complications: toxic megacolon , perforation of
the intestine, significant blood loss; an increased
incidence of colon cancer has also been documented in
patients with ulcerative colitis
Treatment of ulcerative colitis
 Anti-inflammatory drugs and salicylates suppress the
inflammatory response.
 Sulfasalazine
 Nicotine appears to exert a protective effect in ulcerative
colitis but not Crohn’s disease.
 Severe malnutrition may require nutritional
supplementation.
 Surgical resection of diseased bowel may be required.
Disorders of the gall bladder
 The gall bladder is a saclike structure that stores the bile
that is produced by the liver.
 The walls of the gall bladder contain smooth muscle and,
under the stimulus of the duodenal hormone
cholecystokinin , can contract to eject bile down the bile
duct and into the duodenum.
 In the duodenum, bile salts emulsify fats to aid in their
absorption. Bile is composed primarily of water, bile
salts, cholesterol and bilirubin.
Gallstone formation (cholelithiasis)
 Cholelithiasis is the most common disorder of the G.I. system.
 The gallstones that form in the gall bladder are hardened precipitates
of bile that contain predominantly cholesterol.
 The size of gallstones can range from the size of a grain of sand to
several inches in diameter.
 Factors such as aging, excess cholesterol, obesity, sudden dietary
changes or abnormal fat metabolism may contribute to gallstone
formation.
 Gallstones may be detected by a number of techniques including
radiography, ultrasonography and cholecystoscopy.
Manifestations of gallstone formation
 Symptoms of gallstone formation will generally not occur
until the stones have reached sufficient size to block the
bile ducts.
 Acute and severe abdominal pain.
 Nausea, vomiting, fever, chills.
 Jaundice from obstruction of bile outflow.
Treatment
 Surgical removal of gall bladder ( cholecystectomy )
 Endoscopic removal of gallstones
 Lithotripsy — The use of sound waves to break up the
gallstones in the gall bladder
 Low-fat diet for prevention of additional stone formation
Cholecystitis
 Cholecystitis is an acute or chronic inflammation of the
gall bladder.
 It is most commonly caused by the presence of
gallstones in the gall bladder, but may also result from
infection or reduced blood flow to the gall bladder.
 Signs and symptoms are similar to those observed with
cholelithiasis.
 Treatment involves removal of gallstones and antibiotics
for treatment of infection if present.
Thank you